Biomedical subjects

Lloyd H Back

Publications and source records attributed to Lloyd H Back.

7 recordsLinked to original sources

PubMed2006

Characterizing momentum change and viscous loss of a hemodynamic endpoint in assessment of coronary lesions.

Myocardial fractional flow reserve (FFR(myo)) and coronary flow reserve (CFR), measured with guidewire, and quantitative angiography (QA) are widely used in combination to distinguish ischemic from non-ischemic coronary stenoses. Recent studies have shown that simultaneous measurements of FFR(myo) and CFR are recommended to dissociate conduit epicardial coronary stenoses from distal resistance microvascular disease. In this study, a more comprehensive diagnostic parameter, named as lesion flow coefficient, c, is proposed. The coefficient, c, which accounts for mean pressure drop, Delta p, mean coronary flow, Q, and percentage area stenosis, can be used to assess the hemodynamic severity of a coronary artery stenoses. Importantly, the contribution of viscous loss and loss due to momentum change for several lesion sizes can be distinguished using c. FFR(myo), CFR and c were calculated for pre-angioplasty, intermediate and post-angioplasty epicardial lesions, without microvascular disease. While hyperemic c decreased from 0.65 for pre-angioplasty to 0.48 for post-angioplasty lesion with guidewire of size 0.35 mm, FFR(myo) increased from 0.52 to 0.87, and CFR increased from 1.72 to 3.45, respectively. Thus, reduced loss produced by momentum change due to lower percentage area stenosis decreased c. For post-angioplasty lesion, c decreased from 0.55 to 0.48 with the insertion of guidewire. Hence, increased viscous loss due to the presence of guidewire decreased c compared with a lesion without guidewire. Further, c showed a linear relationship with FFR(myo), CFR and percentage area stenosis for pre-angioplasty, intermediate and post-angioplasty lesion. These baseline values of c were developed from fluid dynamics fundamentals for focal lesions, and provided a single hemodynamic endpoint to evaluate coronary stenosis severity.

Biomechanical Phenomena↗

PubMed2006

Guidewire flow obstruction effect on pressure drop-flow relationship in moderate coronary artery stenosis.

To evaluate the local hemodynamic effects of coronary artery balloon angioplasty, computational fluid dynamics was applied to representative stenoses geometry post-angioplasty (minimal lesion diameter d(m) = 1.8mm which produced 64% mean area stenoses) based on a group of patients and measured values of coronary flow reserve (CFR) returning to a normal range (3.6+/-0.3). The computations were at mean flow rates (Q) of 50, 100, 150 and 170 ml/min. The study indicates changes in the hemodynamic conditions due to insertion of a guidewire, which can be used to determine the mean pressure drop (Deltap ) and fall in distal mean coronary pressure (p(r)), and thus give quantitative estimate of uncertainty expected in diagnosis of moderate lesions. The guidewire to minimal lesion diameter ratio is 0.26, causing tighter "artifactual" mean area stenoses of 65.5%. During hyperemia, p(m) dropped to 72 mmHg as compared to 75 mmHg under patho-physiological condition without guidewire. Q(h) (subscript h: hyperemia) decreased from 180 without guidewire to 170 ml/min with the guidewire present. Thus, there was a significant approximately 43% increase in Deltap(h) and a approximately 51% increase in the hyperemic flow resistance (R(h) = Deltap(h)/Q(h)) over the patho-physiological condition. This could cause an overestimation of the severity of the moderate stenoses. Transient and steady flow guidewire surface shear stress was 35-50% higher than corresponding values for arterial wall shear stress. The non-dimensional data given in tabular form may be useful in interpretation of clinical guidewire measurements for moderate lesions of similar geometry and size.

Angioplasty, Balloon, Coronary↗

PubMed2006

Developing pulsatile flow in a deployed coronary stent.

A major consequence of stent implantation is restenosis that occurs due to neointimal formation. This patho-physiologic process of tissue growth may not be completely eliminated. Recent evidence suggests that there are several factors such as geometry and size of vessel, and stent design that alter hemodynamic parameters, including local wall shear stress distributions, all of which influence the restenosis process. The present three-dimensional analysis of developing pulsatile flow in a deployed coronary stent quantifies hemodynamic parameters and illustrates the changes in local wall shear stress distributions and their impact on restenosis. The present model evaluates the effect of entrance flow, where the stent is placed at the entrance region of a branched coronary artery. Stent geometry showed a complex three-dimensional variation of wall shear stress distributions within the stented region. Higher order of magnitude of wall shear stress of 530 dyn/cm2 is observed on the surface of cross-link intersections at the entrance of the stent. A low positive wall shear stress of 10 dyn/cm2 and a negative wall shear stress of -10 dyn/cm2 are seen at the immediate upstream and downstream regions of strut intersections, respectively. Modified oscillatory shear index is calculated which showed persistent recirculation at the downstream region of each strut intersection. The portions of the vessel where there is low and negative wall shear stress may represent locations of thrombus formation and platelet accumulation. The present results indicate that the immediate downstream regions of strut intersections are areas highly susceptible to restenosis, whereas a high shear stress at the strut intersection may cause platelet activation and free emboli formation.

Animals↗

PubMed2005

Delineating the guide-wire flow obstruction effect in assessment of fractional flow reserve and coronary flow reserve measurements.

Hemodynamic analysis was conducted to determine uncertainty in clinical measurements of coronary flow reserve (CFR) and fractional flow reserve (FFR) over pathophysiological conditions in a patient group with coronary artery disease during angioplasty. The vasodilation-distal perfusion pressure (CFR-p(rh)) curve was obtained for 0.35- and 0.46-mm guide wires. Our hypothesis is that a guide wire spanning the lesions elevates the pressure gradient and reduces the flow during hyperemic measurements. Maximal CFR-p(rh) was uniquely determined by the intersection of measured CFR and calculated p(rh) of native and residual epicardial lesions in patients without microvascular disease, during angioplasty. Extrapolation of the linear curve gave a zero-coronary flow mean pressure (p(zf)) of approximately 20 mmHg and a corresponding p(rh) of 55 mmHg in the native lesions, which coincided with the level that causes ischemia in human hearts. On this linear curve, values of CFR and FFRmyo (pathophysiological condition) and CFRg and FFRmyog (in the presence of the guide wire) were obtained in native and residual lesions. A strong linear correlation was found between CFR and CFRg [CFR = CFRg x 0.689 + 1.271 (R2= 0.99) for 0.46 mm and CFR = CFRg x 0.757 + 1.004 (R2= 0.99) for 0.35 mm] and between FFRmyo and FFRmyog [FFRmyo = FFRmyog x 0.737 + 0.263 (R2= 0.99) for 0.46 mm and FFRmyo = FFRmyog x 0.790 + 0.210 (R2= 0.99) for 0.35 mm]. This study establishes a strong correlation between CFR and CFRg and between FFRmyo and FFRmyog, which could be used to obtain the true state of occlusion in the coronary artery during angioplasty.

Angioplasty, Balloon, Coronary↗

PubMed2005

Coupled oxygen transport analysis in the avascular wall of a post-angioplasty coronary artery stenosis.

The coupled oxygen transport in the avascular wall of a coronary artery stenosis is studied by numerically solving the convection-diffusion equations. Geometry, replicating residual stenosis after percutaneous transluminal coronary angioplasty (PTCA), is used for the analysis. Important physiological aspects, such as oxygen consumption in the wall, oxygen carried by the hemoglobin, non-Newtonian viscosity of the blood, and supply of oxygen from the vasa vasorum are included. Mean blood flow rate in the lumen is varied from basal to hyperemic conditions. The results show that the P(O2) in the medial region of the arterial wall is approximately 10 mmHg. The oxygen flux to the wall increases in the flow acceleration region, whereas it decreases at the flow reattachment zone. Near the location of flow separation there is a small rise and a sharp fall in the oxygen flux. The minimum P(O2) in the avascular wall, P(O2, min ), at the point of flow reattachment reduces to approximately 6 mmHg for a 300 micron wall thickness. For a thinner wall of 200 micron, the P(O2, min ) at the location of flow reattachment increases to 6 times that of a 300 micron wall. The P(O2, min ) in the wall decreases by 60% when volumetric oxygen consumption is increased by 30% for the same avascular wall thickness.

Angioplasty, Balloon, Coronary↗

PubMed2003

Physiological flow analysis in significant human coronary artery stenoses.

To evaluate the local hemodynamics in flow limiting coronary lesions, computational hemodynamics was applied to a group of patients previously reported by Wilson et al. (1988) with representative pre-angioplasty stenosis geometry (minimal lesion size d(m)=0.95 mm; 68% mean diameter stenosis) and with measured values of coronary flow reserve (CFR) in the abnormal range (2.3+/-0.1). The computations were at mean flow rates (Q) of 50, 75 and 100 ml/min (the limit of our converged calculations). Computed mean pressure drops Deltap were approximately 9 mmHg for basal flow (50 ml/min), approximately 27 mmHg for elevated flow (100 ml/min) and increased to an extrapolated value of approximately 34 mmHg for hyperemic flow (115 ml/min), which led to a distal mean coronary pressure p(rh) of approximately 55 mmHg, a level known to cause ischemia in the subendocardium (Brown et al., 1984), and consistent with the occurrence of angina in the patients. Relatively high levels of wall shear stress were computed in the narrow throat region and ranged from about 600 to 1500 dyn/cm(2), with periodic (phase shifted) peak systolic values of about 3500 dyn/cm(2). In the distal vessel, the interaction between the separated shear layer wave, convected downstream by the core flow, and the wall shear layer flow, led to the formation of vortical flow cells along the distal vessel wall during the systolic phase where Reynolds numbers Re(e)(t) were higher. During the phasic vortical mode observed at both basal and elevated mean flow rates, wide variations in distal wall shear stress occurred, distal transmural pressures were depressed below throat levels, and pressure recovery was larger farther along the distal vessel. Along the constriction (convergent) and throat segments of the lesion the pulsatile flow field was principally quasi-steady before flow separation occurred. The flow regimes were complex in the narrow mean flow Reynolds number range Re(e)=100-230 and a frequency parameter of alphae=2.25. The shear layer flow disturbances diminished in strength due to viscous damping along the distal vessel at these relatively low values of Re(e), typical of flow through diseased epicardial coronary vessels. The distal hyperemic flow field was likely to be in an early stage of turbulent flow development during the peak systolic phase.

Blood Flow Velocity↗

PubMed2003

Effects of diagnostic guidewire catheter presence on translesional hemodynamic measurements across significant coronary artery stenoses.

This study gains insight on the nature of flow blockage effects of small guidewire catheter sensors in measuring mean trans-stenotic pressure gradients Deltap across significant coronary artery stenoses. Detailed pulsatile hemodynamic computations were made in conjunction with previously reported clinical data in a group of patients with clinically significant coronary lesions before angioplasty. Results of this study ascertain changes in hemodynamic conditions due to the insertion of a guidewire catheter (di=0.46 mm) across the lesions used to directly determine the mean pressure gradient (Deltap) and fall in distal mean coronary pressure (pr). For the 32 patient group of Wilson et al. [1988] (minimal lesion diameter dm=0.95 mm; 90% mean area stenosis; proximal measured coronary flow reserve (CFR) of 2.3 in the abnormal range) the diameter ratio of guidewire catheter to minimal lesion was 0.48, causing a tighter "artifactual" mean area stenosis of 92.1%. The results of the computations indicated a significant shift in the Deltap-Q relation due to guidewire induced increases in flow resistances (R=Deltap/Q) of 110% for hyperemic flow, a 35% blockage in hyperemic flow (Qh) and a phase shift of the coronary flow waveform to systolic predominance. These alterations in flow resulted in a fall in distal mean coronary pressure (at lower mean flow rates) below the patho-physiological range of prh approximately 55 mmHg, which is known to cause ischemia in the subendocardium (Brown et al. [1984]) and coincides with symptomatic angina. Transient wall shear stress levels in the narrow throat region (with flow blockage) were of the order of levels during hyperemic conditions for patho-physiological flow. In the separated flow region along the distal vessel wall, vortical flow cells formed periodically during the systolic phase when instantaneous Reynolds numbers Ree(t) exceeded about 110. For patho-physiological flow without the presence of the guidewire these vortical flow cells were much stronger than in the more viscous flow regime with the guidewire present. The non-dimensional pressure data given in tabular form may be useful in interpretation of guidewire measurements done clinically for lesions of similar geometry and severity.

Angioplasty, Balloon, Coronary↗